Valvular Heart Diseases PDF

Disorders of the Cardiac Valves I ILOs At the end of this session, the student will be able to: Identify the common causes of valves dysfunction. Understand the pathophysiology and the subsequent hemodynamic changes of valvular regurgitation and stenosis. Recognize...

Disorders of the Cardiac Valves I ILOs At the end of this session, the student will be able to: Identify the common causes of valves dysfunction. Understand the pathophysiology and the subsequent hemodynamic changes of valvular regurgitation and stenosis. Recognize the symptoms and signs of the different valvular lesions. Explain how to diagnose valvular lesions. Outline the management plan for each disease. I. Mitral Valve Disease A. Mitral Regurgitation (MR) Anatomy of the mitral valve The mitral valve apparatus is composed of: 1.The mitral annulus. 2. The leaflets comprise a large anterior and a small posterior leaflet. 3. The chordae tendineae. 4. The papillary muscles and the adjacent LV wall. Abnormalities in one or more of these 4 structures can cause mitral valve regurgitation. This regurgitation could be either acute or chronic. Causes of MR: Chronic Acute Rheumatic fever Papillary muscle rupture in Ischemic heart disease due to STEMI Papillary muscle dysfunction. Chordal rupture as in mitral Cardiomyopathy valve prolapse. Mitral valve prolapse. Infective endocarditis Page 1 of 23  Calcification of mitral annulus. Infective endocarditis with Congenital as cleft mitral valve. cusp perforation or chordal rupture Chest trauma Pathophysiology: -Acute severe mitral regurgitation (MR) leads to acute LV volume overload with no sufficient time for ventricular dilatation, so LV diastolic pressure markedly increased and transmitted to left atrium then pulmonary circulation leading to acute pulmonary edema. -Chronic MR is a slowly progressive condition that starts with minimal regurgitation and increases slowly over years, so the LV has sufficient time to dilate to accommodate the excess diastolic volume without increase in LV diastolic pressure. -During systole, blood regurgitates from left ventricle to left atrium leading to increased left atrial volume and pressure. The left atrium dilates to accommodate excess blood volume and increases the left atrial pressure. -Later, the LA dilatation will be not sufficient for the progressively increasing regurgitation volume and the LA pressure will increase more and transmits back to the pulmonary circulation leading to pulmonary congestion and later pulmonary hypertension with subsequent RV affection. -Progressive left ventricular dilatation causes dilatation of the mitral annulus and aggravates mitral regurgitation. Page 2 of 23 -Left atrial enlargement predisposes the patient to atrial fibrillation. Complications: 1- Atrial fibrillation: it aggravates the symptoms of pulmonary venous congestion and increases the risk of thrombosis and systemic embolization. 2- The congested respiratory tract predisposes for recurrent pulmonary infections. 3- Development of pulmonary hypertension and right heart failure. 4- Infective endocarditis is relatively common. Clinical picture: Patients with chronic, severe mitral regurgitation may remain asymptomatic for years because of the compensatory ventricular and atrial dilation. Symptoms: -Acute severe MR usually presents with severe dyspnea due to acute pulmonary edema. -In chronic MR when symptoms occur, they usually increase slowly, fatigue perhaps due to low cardiac output may be the first complaint followed by dyspnea on exertion, paroxysmal nocturnal dyspnea or even orthopnea. Signs: -Signs of left ventricular dilatation (hyper dynamic localized apex with +ve thrust that is shifted downward and outward) due to LV volume overload. -Muffled first heart sound, P2 may be accentuated. -Third heart sound S3 may be heard. -Harsh pan‐systolic murmur over the apex, propagated to axilla, increases with isometric exercise. -In case of severe mitral regurgitation, short functional mid‐diastolic rumbling murmur may be heard due to excessive blood flow across the valve. Investigations: ECG: 1. You may find P mitrale if atrial fibrillation is not present. 2. Left ventricular hypertrophy in severe MR. Chest radiography: 1. Marked left atrial enlargement. Page 3 of 23  2. May also be evidence of LV enlargement. 3. Evidence of pulmonary vascular dilatation and pulmonary edema develops when there is LV failure. Echocardiography 1. Visualization of mitral leaflets morphology and function. 2. Assessment of the degree of mitral regurgitation. 3. Measuring Left ventricular dimensions and functions. 4. Checking for the presence of pulmonary hypertension. Cardiac Catheterization: Preoperative coronary artery evaluation in males above 40 years and females above 50 years or presence of coronary risk factors. Treatment of mitral regurgitation: - Acute MR: afterload reduction with vasodilators, e.g., intravenous nitroprusside and nitroglycerin together with IV diuretics reduces the regurgitated flow and the pulmonary pressure until definitive surgical treatment is feasible. -Assisted ventilation in case of acute pulmonary edema and severe hypoxia. -Chronic MR: -The management of these patients is focused on deciding on the appropriate timing of surgery before the development of irreversible left ventricular dysfunction. Medical treatment includes: 1. Alleviating pulmonary congestion with diuretics. 2. Treating atrial fibrillation: oral anticoagulation in addition to ventricular rate control with beta blockers or digitalis. 3. Long‐term secondary prophylaxis against rheumatic fever, preferentially with long-acting penicillin is recommended for all patients with rheumatic etiology. 4. Antibiotic prophylaxis against infective endocarditis is recommended prior to high-risk procedures. -Patients should be followed up every 6 to 12 months to assess for symptoms and to measure left ventricular size, function, and severity of MR by echocardiography. Surgical treatment indications: Symptomatic patients with severe primary MR Asymptomatic patients with severe primary MR and evidence of LV dysfunction (LV ejection fraction < 60%) Page 4 of 23  Relative indication: Asymptomatic severe MR with severe LV dilatation (with normal EF) or pulmonary hypertension or development of atrial fibrillation The two available surgical options are mitral valve repair and mitral valve replacement. Mitral valve repair is the procedure of choice if technically feasible. * Mitral Valve Prolapse Mitral valve prolapse (MVP) is the systolic billowing (bulging) of one or both mitral leaflets into the left atrium during systole. The tissue of the mitral valve leaflets and chordae are abnormally redundant. Those with mitral valve prolapse may not have any regurgitation or they may have a range of severity from mild to severe regurgitation. It is more common in females. Clinical picture: Most patients with MVP are asymptomatic. Multiple nonspecific symptoms e.g., atypical chest pain, dyspnea, and palpitations. The classic findings of MVP on physical examination are a mid-systolic click, with a mid to late systolic murmur, heard best at the cardiac apex. Management: Beta blockers are useful for alleviating symptoms of palpitations and chest pain in certain patients. In MVP patients with severe mitral regurgitation, the indications for mitral valve surgery are like those for patients with other causes of severe regurgitation. When surgery is required, mitral valve repair is usually the procedure of choice. B. Mitral Stenosis (MS) Etiology: 1. Rheumatic fever is the main cause of mitral stenosis. 2. In the elderly: severe calcification of the mitral annulus. 3. Very rare: congenital parachute mitral valve in young children. Pathophysiology Page 5 of 23 -The normal area of the mitral valve orifice is about 4 to 6 cm 2. When the mitral valve area goes below 2.0 cm2, the valve causes obstruction to the flow of blood into the left ventricle, creating a diastolic pressure gradient across the mitral valve. -The LV will receive less amount of blood and left atrial pressure increases, the left atrium dilates then the left atrial pressure is transmitted back to the pulmonary circulation causing pulmonary venous hypertension and symptoms of pulmonary congestion starts to appear. -Later, pulmonary arterial hypertension occurs resulting in RV dilatation and 2ry tricuspid regurgitation with systemic venous congestion. -Left ventricular filling across the stenotic mitral valve requires adequate diastolic time and adequate atrial contraction. These patients are very sensitive to tachycardias and atrial fibrillation (loss of atrial kick) with rapid deterioration of symptoms with onset of AF. -Low cardiac output can occur late with severe stenosis or severe pulmonary hypertension. Complications: a. Atrial fibrillation (AF): it aggravates the symptoms of pulmonary venous congestion and might precipitate acute pulmonary edema. Also, AF increases the risk of thrombosis and systemic embolization. b. The congested respiratory tract predisposes for recurrent pulmonary infections. c. Development of pulmonary hypertension and right heart failure. Page 6 of 23  d. Pulmonary embolism and pulmonary infarction especially when the disease is advanced. e. Frank hemoptysis from rupture of dilated bronchial or pulmonary veins (bronchopulmonary apoplexy). f. Infective endocarditis is rare in mitral stenosis. Q- What are the causes of hemoptysis in mitral stenosis? Symptoms 1. The patient may remain asymptomatic. However, patients may decompensate during pregnancy or atrial fibrillation. 2. Commonly, patients suffer from symptoms of pulmonary congestion (mainly dyspnea, PND and orthopnea). Sometimes they suffer from hemoptysis. 3. Symptoms of systemic venous congestion like pain and tenderness in the right hypochondrium secondary to hepatic congestion and bilateral lower limbs edema. 4. Symptoms of low COP in severe cases, like easy fatigue. Physical examination 1. Malar flush may be present. 2. Signs of pulmonary congestion and systemic venous congestion 3. Local examination: 4. Signs of RV dilatation, pulmonary hypertension and tapping apex (palpable S1). 5. An apical diastolic thrill might be felt. 6. Auscultatory findings: a. Accentuated S1. b. Opening snap may be present. c. Mid-diastolic low pitch rumbling murmur with presystolic accentuation, localized to the apex, best heard in left lateral position with the bell of stethoscope, increase with exercise. d. The presystolic accentuation of MS murmur is absent in patients with AF. e. The longer the duration of the diastolic murmur is, the more severe the stenosis is. f. Accentuated P2 and pan systolic murmur of tricuspid regurgitation may be present. Diagnosis A. ECG: Page 7 of 23 1. If sinus rhythm is present, there are signs of left atrial dilatation (P-mitrale), or of pulmonary hypertension (P-pulmonale). 2. Atrial fibrillation is common. 3. Evidence of right ventricular hypertrophy develops in cases with severe pulmonary hypertension. B. Chest radiography: 1. Selective enlargement of left atrial enlargement 2. A normal or small left ventricle 3. Radiological pictures of pulmonary congestion or even pulmonary edema may be seen. 4. The pulmonary artery, right ventricle and occasionally, the right atrial enlargement may also be seen when there is pulmonary hypertension. 5. Signs of pulmonary congestion and pulmonary hypertension. 6. Signs of right ventricular hypertrophy (if pulmonary hypertension develops). C. Echocardiography: ▪ Characteristic findings of MS include valve thickening; the valve might be calcified. There are restricted valve opening, anterior leaflet doming, and fusion of the leaflets at the commissures. ▪ The trans‐mitral gradient as measured by Doppler echocardiography and mitral valve area are the gold standard in the evaluation of the severity of mitral stenosis. Degree of Mean Valve mitral gradient area stenosis Mild 1.5 cm2 Moderate 5 ‐ 10 1.0 ‐ 1.5 cm2 Severe > 10 < 1.0 cm2 ▪ Trans esophageal echocardiography (TEE) is superior to transthoracic echocardiography (TTE) at identifying left atrial thrombus in patients who are being considered for percutaneous mitral balloon valvotomy or atrial fibrillation cardioversion. Page 8 of 23  D. Cardiac Catheterization: Preoperative coronary artery evaluation in males above 40 years and females above 50 years or presence of coronary risk factors. Medical treatment: 1. Alleviating pulmonary congestion with diuretics. 2. Beta blockers slow the heart rate and increase the diastolic time for better LV filling. 3. Treating atrial fibrillation: oral anticoagulation in addition to ventricular rate control with beta blockers, calcium channel antagonists (verapamil or diltiazem) and digitalis. 4. Long‐term secondary prophylaxis against rheumatic fever, preferentially with long-acting penicillin, is recommended for all patients with rheumatic mitral stenosis. Indication of intervention: i. Absolute indication: Patients with symptomatic moderate to severe MS ii. Relative indication: Patients with asymptomatic severe MS with pulmonary hypertension or atrial fibrillation iii. Options of intervention: 1. Percutaneous mitral balloon valvotomy (PMBV): balloon introduced from the femoral vein to RA then trans-septal to LA is positioned and inflated across the stenotic valve to split the fused commissures. Contra-indication includes: a. Severe valve calcification b. Severe valve thickening and fibrosis c. Marked sub-valvular affection. d. Presence of more than mild mitral regurgitation e. Presence of left atrial thrombi 2. Surgical treatment: in case of contraindication to PMBV or its failure, or the presence of concomitant indication of open-heart surgery (coronary artery disease or another valve lesion) a. Surgical repair (open commissurotomy) if feasible b. Mitral valve replacement (MVR) with tissue valve or mechanical valve. Page 9 of 23  2-Tricuspid Valve Disease. Anatomy of the tricuspid valve: The tricuspid valve apparatus includes leaflets or cusps, chordae, papillary muscles, and tricuspid annulus. In general, the tricuspid valve has three distinct leaflets described as septal, anterior, and posterior. Etiology of tricuspid valve disease Tricuspid valve disease is generally classified as primary (intrinsic) valve pathology or secondary (functional). Functional tricuspid valve regurgitation is secondary to left‐heart disease causing pulmonary hypertension with subsequent RV enlargement and TV annular dilatation. Causes of Primary Tricuspid Valve Diseases: 1. Rheumatic valve disease, generally in association with rheumatic mitral disease. 2. Infective endocarditis (especially IV drug abuse and indwelling venous lines) 3. Carcinoid heart disease. 4. Congenital (Ebstein anomaly) causing TV regurgitation. Clinical Presentations Symptoms Generally, the symptoms of left heart disease predominate in those with secondary tricuspid valve disease. The symptoms specific to advanced tricuspid valve disease are related to: o Decreased cardiac output, for example, fatigue. o Right atrial hypertension, for example, liver congestion resulting in right upper quadrant discomfort, or gut congestion with symptoms of dyspepsia, indigestion, or fluid retention with leg edema and ascites. Physical Signs These include signs related to tricuspid valve disease and those secondary to chronic venous congestion, leg edema and ascites. Page 10 of 23 Tricuspid stenosis Tricuspid regurgitation Slow Y descent and prominent "a" Prominent C‐V wave (systolic neck wave. venous pulsations) Liver is enlarged with a firm edge. Left parasternal pulsations or lift from right It shows presystolic pulsations. ventricular enlargement. RV apex. Auscultation reveals a diastolic Liver shows systolic expansile pulsations. rumble with inspiratory accentuation. It is enlarged and often tender. Cardiac auscultation reveals a holosystolic murmur which is augmented with inspiration (Carvallo’s sign). Diagnosis -ECG and Chest X ray signs of RA and RV dilatation -Echocardiography: o Evaluate the valve pathology. o Differentiate 1ry versus 2ry valve lesions. o Assess the severity of valve dysfunction. o Estimate the pulmonary artery systolic pressure. o RV dimensions and function. o Other valves function. Treatment: o Diuretics may decrease systemic congestion. o Surgical Repair of TV (annuloplasty) is commonly used for concomitant TR with left sided lesion. 3. Aortic Valve Disease Anatomy of aortic valve: The aortic valve is located between the left ventricular outflow tract and the ascending aorta. In most cases, it is composed of three semilunar cusps. However, in some cases, it can be bicuspid. The aortic valves are shaped and function like an 'umbrella'. The cusps project into the artery and are completely open during systole. During the relaxation of the myocardial wall (diastole), the elastic wall of the aorta pushes the blood back into Page 11 of 23  the heart. However, the shape of the cusps and the aortic root activate the cusps and completely close the aortic valve. This process prevents the reverse blood flow into the left ventricle. A. Aortic Regurgitation (AR) Causes of chronic aortic valve regurgitation: 1. Aortic root dilation: aortic aneurysm and Marfan’s syndrome 2. Post-inflammatory: Rhematic fever, infective endocarditis and ankylosing spondylitis. NB. Acute aortic valve regurgitation could occur secondary to cusp perforation as in cases of infective endocarditis and aortic dissection. In such cases the patient will present with acute left ventricular failure. Pathophysiology of aortic valve regurgitation: Clinical picture of aortic valve regurgitation: Symptoms The development of symptoms is generally due to pulmonary congestion. Page 12 of 23  Initial symptoms include dyspnea on exertion and a decrease in exercise tolerance. Later, symptoms of orthopnea and paroxysmal nocturnal dyspnea usually occur as LV systolic function begins to decline. Angina (also nocturnal angina) may uncommonly occur regardless of obstructive coronary artery disease owing to decreased myocardial perfusion pressure causing subendocardial ischemia. Signs: AR is characterized by a hyperdynamic pulse and wide pulse pressure as a result of a brisk systolic upstroke (caused by increase in LV SV) followed by a rapid diastolic collapse (caused by reversal of flow in the aorta). It is best appreciated by raising the arm abruptly and feeling the radial pulse (Water Hammer pulse). This hyperdynamic pulse was thought to result in the many classic eponymous signs of AR. What are the peripheral signs of chronic aortic valve regurgitation? 1-Water-Hammer Pulse: abrupt distension and quick collapse on palpation of the peripheral arterial pulse 2- Pistol-shot (Traube sign): booming systolic and diastolic sounds auscultated over the femoral artery 3-Corrigan Sign: vigorous carotid pulsations. 4-Duroziez sign: systolic murmur over the femoral artery with proximal compression of the artery and diastolic murmur over the femoral artery with distal compression of the artery. 5-Muller sign: visible systolic pulsations of the uvula 6-Quincke sign: visible pulsations of the fingernail bed with light compression of the fingernail 7-Hills sign: popliteal cuff systolic blood pressure 40 mmHg higher than brachial cuff systolic blood pressure Local cardiac examination Hyperdynamic LV apical impulse S4, S3 Gallop Apical Rumble (Austin flint murmur ) Diastolic Decrescendo Blowing Murmur Diagnosis of aortic regurgitation:  ECG: Signs of left ventricular hypertrophy, left atrial enlargement. Page 13 of 23   Chest X-ray: Cardiomegaly, ascendant Aorta aneurysm.   Echocardiography: It is considered the gold standard to assess the etiology, severity and haemo-dynamic consequences of aortic regurgitation.  Cardiac Catheterization: Generally, coronary catheterization is indicated to assess coronary anatomy pre-AVR in all patients >50 years of age. Invasive aortography may be useful to assess the degree of AR when echocardiography and clinical findings are discordant. Management of aortic regurgitation: Medical management: The primary goal is to alleviate symptoms and to treat associated conditions such as systemic hypertension and heart failure. Vasodilators (dihydropyridine calcium channel blockers, angiotensin-converting enzyme (inhibitors/angiotensin receptor blockers, or hydralazine) are used for LV afterload reduction. They are indicated in severe chronic AR with (1) symptoms, (2) LV dysfunction, or (3) hypertension. They are generally used if the patient is not an operative candidate or while the patient is waiting for surgical AVR. Page 14 of 23 Surgical therapy In appropriate patients, AV surgery remains the only definite treatment for AR. Surgical techniques include repair or replacement (mechanical or bio-prosthesis). B. Aortic Stenosis (AS) Etiology of aortic valve stenosis: 1. Senile calcific aortic stenosis: age-related degenerative calcific disease. Most common. 2. Congenital bicuspid aortic valve disease. 3. Post inflammatory : rheumatic heart disease. Pathophysiology : Page 15 of 23 Clinical picture of aortic valve stenosis: Symptoms The 3 cardinal manifestations of AS are exertional dyspnea, angina and syncope. Symptoms typically begin at age 50 to 70 years with bicuspid aortic valve stenosis and in those older than 70 with calcific stenosis of a trileaflet valve. The most common clinical presentation in patients with a known diagnosis is a gradual decrease in exercise tolerance, fatigue, or dyspnea on exertion. Angina is a frequent symptom of patients with severe AS and usually resembles the angina observed in patients with coronary artery disease (CAD) in that it is usually precipitated by exertion and relieved by rest. Signs General Pulse: slow rising and weak (parvus), delayed peak (tardus), small volume Lung fine basal crepitation Cardiac examination Apex − may shift to left (downward & outside due to LVH) − Heaving apex A systolic thrill: at the base of the heart A2 component of S2 might be absent/ soft/normal. Prominent S4 Ejection systolic murmur rough character best heard in Rt. 2nd ICS radiates to neck Diagnosis of aortic stenosis:  ECG : An electrocardiogram is useful to confirm heart rhythm, assess for left ventricular hypertrophy, and detect underlying conduction system disease (a common comorbid finding in patients with AS) Page 16 of 23   Chest X-ray: Cardiomegaly, calcifications of aortic valve.  Echocardiography: It is considered the gold standard to assess the etiology, severity and haemo-dynamic consequences of aortic stenosis.  Cardiac Catheterization: If there are inconclusive, noninvasive data, particularly in symptomatic patients, or if there is a discrepancy between the noninvasive tests and clinical findings, a hemodynamic cardiac catheterization should be considered Management of aortic stenosis: A- MEDICAL TREATMENT In short, there is no medical therapy currently proven to alter the natural history of AS. Nonetheless, guideline-directed medical therapy is advised for common comorbidities such as hyperlipidemia, diabetes mellitus, and hypertension. Antihypertensive medications should be initiated at low dose and gradually titrated, particularly in patients with severe AS. Patients with severe AS and severe decompensated heart failure may benefit from medical stabilization using careful afterload reduction prior to urgent aortic valve replacement. B- SURGICAL/PERCUTANEOUS INTERVENTION *Aortic valve replacement is indicated for symptomatic patients with low- or intermediate-risk for cardiac surgery. *Transcatheter aortic valve implantation (TAVI) is indicated for patients with prohibitive surgical risk with a life expectancy >12 months or as an alternative procedure for patients deemed at intermediate or high surgical risk as assessed by a Heart Valve Team. 4. Pulmonary Valve Disease Anatomy: The pulmonary valve is a trileaflet valve that lies anterior and to the left of the aortic valve and separates the right ventricular outflow tract (RVOT) from the pulmonary trunk. The three pulmonary leaflets are semilunar in shape and are thinner than the aortic leaflets. Page 17 of 23 Etiology: A. Pulmonary regurgitation (PR): A mild degree of PR is a common finding in healthy adults. In adults, the most common cause of moderate PR is pulmonary hypertension. Other causes of PR are rare and include endocarditis, rheumatic heart disease, carcinoid, pulmonary artery aneurysm. B. Pulmonary stenosis (PS): It can occur at three levels (valvular, sub valvular and supra valvular). Congenital PS is by far the most frequent cause. PATHOPHYSIOLOGY: A- Pulmonary regurgitation: PR causes volume overload on the RV, the severity of which depends on the degree and duration of the regurgitant flow. The low pulmonary vascular resistance allows blood to easily pass through the lungs despite severe PR, thus limiting significant RV volume overload and allowing this lesion to be tolerated for longer periods. Ultimately, severe chronic RV volume overload leads to RV dilatation and dysfunction with resultant right- sided heart failure symptoms. B- Pulmonary stenosis: The RV initial response to the pressure overload created by PS is an increase in its wall thickness with resultant RV hypertrophy. If left uncorrected, depending on the severity and chronicity of the pressure overload, RV dilatation and dysfunction may occur. Clinical manifestation: Pulmonary regurgitation: The vast majority of patients are asymptomatic. Symptoms develop when RV dilatation and dysfunction occur. Symptoms and signs of RV failure include dyspnea on exertion, fatigue, lower extremity edema, and rarely ascites. Pulmonary stenosis: The presence of symptoms depends on the severity of obstruction and the degree of RV myocardial compensation. Symptoms thus vary from mild exertional dyspnea to a full picture of right-sided heart failure. Page 18 of 23 Cardiac examination: Pulmonary regurgitation Typically, the murmur of PR is diastolic, decrescendo, best heard in the left upper sternal region. Pulmonary stenosis: A systolic ejection murmur is heard with maximal intensity at the left upper sternal border and increases in intensity with inspiration. Diagnosis: ECG: signs of right ventricular hypertrophy, P pulmonale. Chest X ray: Enlarged right ventricular and atrial shadows. Pulmonary oligemia is present in pulmonary stenosis. Echocardiography: gold standard to assess severity and etiology. Right heart catheterization has diagnostic and therapeutic role. Management: Medical treatment has a limited role. Pulmonary regurgitation: valve replacement is considered in severe lesion with right ventricular dysfunction. Pulmonary stenosis: ballon valvuloplasty is of choice if the anatomy is suitable. _____________________________________________________________________ Page 19 of 23  Prosthetic Heart Valves: Broadly, prosthetic valves are divided into those made of biologic tissue (porcine, bovine, even equine) and those that are mechanical. Types of prosthetic valves: A- Bioprosthetic valve: They may be surgical or transcatheter implanted. They are either stented (figure A), stentless (figure B) or percutaneous bioprosthetic valve (figure C). They do not require lifelong anticoagulation with Warfarin. However, bio-prosthesis can show structural degeneration leading to either stenosis or regurgitation after several years. Page 20 of 23  B- Mechanical valve: They are made of metallic material; thus have more durability but need lifelong anticoagulation with warfarin. The older version like Caged ball (figure C) and single tilting disc (figure B) are no longer used. Currently in use are bi-leaflets valves (figure A). They are surgically implanted. Page 21 of 23 Complications of prosthetic valves: a- Valve thrombosis: Mainly complicate mechanical valve rather than bio-prosthesis. It happens when there is no adequate anticoagulation with sub therapeutic dosing of warfarin or concomitant hypercoagulable state like pregnancy. Page 22 of 23 The recommended target INR for a mechanical prosthetic valve in the mitral position is 2.5-3.5. While the recommended INR for a mechanical prosthesis in the aortic position is 2.0-3.0. First line management for an obstructive prosthetic valve thrombosis, is a redo surgery. If not available, the second choice will be thrombolytic therapy. b- Infective endocarditis Patients with prosthetic valves are at high for infective endocarditis. Thus, they should receive prophylactic antibiotics before special procedures. Prosthetic valve endocarditis still results in significant morbidity and mortality. Endocarditis that occurs within the first 60 days of valve implantation is generally acquired from the hospital setting, and the most common agent is Staphylococcus aureus. Endocarditis that develops after 60 days but within the first year of valve implantation (two-thirds of cases occur within the 1st year) represents a mix between health care–acquired infection and community-acquired infection. Coagulase-negative Staphylococcus is the most common pathogen. Infection that develops after the first year is typically community acquired, and the pathogens resemble those of native valve endocarditis. C- Bioprothesis degeneration: leading to either stenosis or regurgitation after several years. NB: Transesophageal echocardiography (TEE) is the imaging method of choice to assess prosthetic valves dysfunction and its related complications. Page 23 of 23